Evidence map›Paper›PMID 41571095›Full record

ArticleCellular and molecular gastroenterology and hepatology2026

Blautia coccoides Alleviates Acute Pancreatitis via Bile Salt Hydrolase-mediated Deoxycholic Acid Production and Farnesoid X Receptor Signaling.

Yang Fu, Binqiang Xu, Wenfei Qin, Wei Xiao, Huizhen Huang, Jia Hu, Mengyan Cui, Qixiang Mei, Junjie Fan, Chunlan Huang and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular and molecular gastroenterology and hepatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Modulating Bile Acid Metabolism: The Role of Blautia coccoides in Acute Pancreatitis.Cellular and molecular gastroenterology and hepatology · 2026
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Yang FuDepartment of Gastroenterology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Institute of Pancreatic Diseases, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Department of Gastroenterology, Northern Jiangsu People's Hospital Affiliated to Yangzhou University, Yangzhou, China.
Binqiang XuDepartment of Gastroenterology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Institute of Pancreatic Diseases, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Wenfei QinSchool of Agriculture and Biology, Shanghai Jiao Tong University, Shanghai, China.
Wei XiaoSchool of Health Science and Engineering, Shanghai Engineering Research Center of Food Microbiology, University of Shanghai for Science and Technology, Shanghai, China.
Huizhen HuangDepartment of Gastroenterology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Institute of Pancreatic Diseases, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jia HuDepartment of Gastroenterology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Institute of Pancreatic Diseases, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Mengyan CuiDepartment of Gastroenterology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Institute of Pancreatic Diseases, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Qixiang MeiDepartment of Gastroenterology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Institute of Pancreatic Diseases, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Junjie FanDepartment of Gastroenterology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Institute of Pancreatic Diseases, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Electronic address: 956937215@qq.com.
Chunlan HuangDepartment of Gastroenterology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Institute of Pancreatic Diseases, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Electronic address: chunlan.huang@shgh.cn.
Yue ZengDepartment of Gastroenterology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Institute of Pancreatic Diseases, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Electronic address: carrie_1004@sjtu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND &

aimsGut dysbiosis is involved in the pathogenesis of acute pancreatitis (AP), yet therapeutic interventions remain limited. Our previous study found the relative abundance of Blautia is significantly decreased in AP, suggesting its protective role.

methodsWe quantified Blautia coccoides in patients with AP and tested its effects in AP mice. Untargeted metabolomics identified deoxycholic acid. Farnesoid X receptor (FXR) signaling was tested with agonists and antagonists. 16S rRNA sequencing was applied to explore changes of gut microbiota. In vitro co-culture assays verified the microbial interaction. The role of bile salt hydrolase (BSH) was confirmed through experiments involving inhibitor and BSH-engineered E coli.

resultsWe observed reduced B coccoides in patients with AP that correlated with disease severity. In AP mice, gavage of B coccoides mitigated pancreatic and intestinal injury. Untargeted metabolomics revealed the increased level of deoxycholic acid (DCA), which could reproduce the protective phenotype of B coccoides. We further found that DCA acts primarily within the intestine to activate FXR, which suppressed pro-inflammatory nuclear factor κB (NF-κB) and NLRP3 pathways. FXR activation also induced production of fibroblast growth factor 15 (FGF15), which protected pancreatic acinar cells. 16S rRNA sequencing showed that B coccoides increased the abundance of BSH-producing genera, Parabacteroides and Bacteroides. In vitro, B coccoides supernatant promoted the growth of representative strains from these genera. Inhibition of BSH abrogated the protective effects of B coccoides, whereas administration of BSH-engineered E coli could ameliorate AP.

conclusionsB coccoides alleviated AP by reshaping gut microbiota composition, enhancing BSH-mediated DCA production, and activating the intestinal FXR-FGF15 signaling to suppress inflammation.

Indexed as

AmidohydrolasesDeoxycholic AcidDysbiosisPancreatitisReceptors, Cytoplasmic and NuclearAnimalsDisease Models, AnimalGastrointestinal MicrobiomeHumansMaleMiceMice, Inbred C57BLReceptor, Farnesoid X-ActivatedSignal TransductionAmidohydrolasescholoylglycine hydrolaseDeoxycholic AcidReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearAcute PancreatitisBile Salt HydrolaseBlautia coccoidesDeoxycholic AcidFarnesoid X Receptor

Identifiers

PMID41571095
PMCPMC12990378

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.